title: Transcriptomic analysis of Streptomyces coelicolor Cvn8 mutants on ISP2 agar in isolation or in an interaction

city: Berkeley

first: Matthew

last: Traxler

state: CA

address: 311 Koshland Hall

department: Plant and Microbial Biology

institute: University of California, Berkeley


title: A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [copy_number]

status: Public on Sep 08 2021

city: Montpellier

first: romain

last: forey

address: 142 avenue de la Cardonille

country: France

institute: IGH

type: Genome variation profiling by high throughput sequencing

summary: Upon replication stress, the Mec1ATR kinase triggers the downregulation of transcription, reducing the level of RNA polymerase on chromatin to facilitate replication fork progression. We identify a hydroxyurea-induced phosphorylation site at Mec1-S1991 that contributes to the eviction of RNAPII and RNAPIII during replication stress. The non-phosphorylatable mec1-S1991A mutant reduces replication fork progression genome-wide and compromises survival on hydroxyurea. This defect can be suppressed by destabilizing chromatin-bound RNAPII with a Rpb3-TAP fusion, suggesting that lethality arises from replication-transcription conflicts. Coincident with a failure to repress gene expression, highly transcribed genes like GAL1 persist at nuclear pores in mec1-S1991A cells. Consistently, we find pore proteins and several components controlling RNAPII and RNAPIII transcription are phosphorylated in a Mec1-dependent manner, suggesting that Mec1-S1991 phosphorylation limits conflicts between replication and either RNA polymerase complex. We further show that Mec1 contributes to reduced RNAPII occupancy on chromatin during an unperturbed S phase.

overall_design: NGS-based analysis of origin activity in HU-arrested S. cerevisiae cells

first: Verena

last: Hurst

first: Kiran

last: Challa

first: Felix

last: Jonas

first: Romain

last: Forey

first: Christoph

middle: D

last: Schmid

first: Naama

last: Barkai

first: Kenji

last: Shimada

first: Susan

middle: M

last: Gasser

first: Jérôme

last: Poli


title: Transcriptomic analysis of Streptomyces coelicolor Cvn8 mutants on ISP2 agar in isolation or in an interaction [2017RNAseqData]

middle: F

country: USA

type: Expression profiling by high throughput sequencing

summary: S. coelicolor spore stocks were diluted to 2x108 cfu/mL and 0.5ul was spotted onto a 60x15mm petri dish with 4ml ISP2 agar, resulting in agar approximately 2 mm thick. For interactions, 0.5 ul of an Amycolatopsis sp. AA4 stock (8x108 cfu/mL) was spotted 0.75 cm away from the S. coelicolor spot. Interactions were grown for 4 days at 30°C, then imaged or harvested for RNA isolation.  Biomass was collected after 4 days of growth at 30°C using a cell scraper. For the patches growing alone, the entire patch was collected and one sample consists of three whole patches combined. For the patches in interactions, only half of the patch, the side closest to the initiator strain, was collected and one sample consists of five half patches. Precaution was taken to not scrape up any of the interacting strain.

overall_design: Bacterial patches grown in isolation or in interactions with Amycolatopsis sp. AA4 for 4 days at 30C on ISP2

first: Bailey

last: Bonet


title: Transient mTOR inhibition rescues 4-1BB-CAR-Tregs from tonic signal-induced dysfunction

status: Public on Sep 07 2021

city: Boston

first: CBDM

last: Lab

state: MA

address: 77 Avenue Louis Pasteur

department: Microbiology and Immunobiology

institute: Harvard Medical School

summary: RNAseq analysis of human CAR-Tregs, bearing CD28 or 4-1BB as a costimulatory domains, initially isolated (before engineering) from peripheral blood of healthy donors

overall_design: CD25+ naive Tregs from healthy donors were sorted, activated, transduced with lentiviral vector for CAR+CD28/4-1BB expression and expanded for 16 days, with a CAR-negative sorting (CD25-NT) or CAR-positive sorting (CD25+28/25+BB) at D11 of culture. At D16 cells were stained and sorted by flow cytometry as DAPI– CD4+CD25+ FVD-EGFR+ or FVD-EGFR- (CD25-NT). 1,000 cells were double-sorted directly into lysis buffer for RNA-seq (Smart-seq2)  library preparation following the standard ImmGen low-input protocol (www.immgen.org). Samples were collected in independent experiments and sequenced in the same RNAseq batch.

first: Baptiste

last: Lamarthée

first: Armance

last: Marchal

first: Soeli

last: Charbonnier

first: Tifanie

last: Blein

first: Juliette

last: Leon

first: Isabelle

last: André

first: Julien

last: Zuber


title: Impaired GR expression in liver disrupts feeding induced gene expression, glucose uptake and glycogen storage

city: Odense

first: Lars

last: Grøntved

address: Campusvej 55

department: Biochemistry and Molecular Biology

country: Denmark

institute: University of Southern Denmark

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The transition from a fasted to a fed state is associated with extensive transcriptional remodeling in hepatocytes facilitated by hormonal- and nutritional-regulated transcription factors. Here, we use a liver-specific glucocorticoid receptor (GR) knock-out (L-GRKO) model and primary hepatocytes to investigate the temporal expression of GR target genes in response to feeding. Interestingly, in addition to the well described fasting-regulated genes, we identify a subset of hepatic feeding-induced genes that requires GR for full expression, adding new insights to hepatic GR function. The GR-controlled feeding-induced genes include Gck encoding the glucokinase, which is important for hepatic glucose uptake, utilization and storage. We show that insulin and glucocorticoids cooperatively regulate Gck expression in primary hepatocytes in a GR-dependent manner. ChIP-seq experiments suggest direct GR regulation of Gck by GR occupancy of the promoter and two putative regulatory regions near the Gck gene (Gck -1kb and Gck -4.6kb). Enhancer-reporter assays and CRISPRi suggest that the 4.6kb upstream GR binding site is a functional Gck enhancer. L-GRKO blunts preprandial and early postprandial Gck expression and GR disruption ultimately affects early postprandial hepatic glucose uptake, phosphorylation and glycogen storage. Collectively, our study demonstrates how GR is positively involved in the hepatic feeding response exemplified in the direct regulation of the feeding-induced transcription of glucokinase, important for hepatic glucose metabolism.

sample_organism:
Mus musculus
Rattus norvegicus

platform_organism:
Mus musculus
Rattus norvegicus

overall_design: Examination of feeding regulated gene expression in liver from C57BL/6 WT and liver specific GR KO mice. Analysis of dex and insulin mediated gene expression in primary hepatocytes

first: Stine

last: Præstholm


title: Swine ileum development at single cell level

city: Qingdao

first: Yong

last: Zhao

state: Shandong

address: 700 Changcheng Road

department: College of Life Sciences

country: China

institute: Qingdao Agricultural University

summary: Different time point piglet ilcum scRNA-seq

overall_design: scRNA-seq of pig cecum at different time points

first: Bohui

last: Xiong

first: Hongfu

last: Zhang

first: Wei

last: Ge

first: Liang

last: Chen

first: Qingshi

last: Meng


title: Study on anti-HBV mechanism of Liuweiwuling Tablet (LWWL) based on transcriptomics

city: Shanghai

first: Tiansheng

last: Xu

address: No. 138 Xinjunhuan Road

institute: OE

summary: Transcriptomics were used to evaluate the possible mechanism and pathway of LWWL against HBV

overall_design: Control:C1 C2 C3; LWWL: L1 L2 L3; TDF: T1 T2 T3

first: Feilin

first: Lanlan

last: Si

first: Yan

last: Yang

first: Yuanhua

last: Li

first: Zhaofang

last: Bai

last: Liu

first: Xiaohe

last: Xiao


title: Morc3 silences endogenous retroviruses by enabling Daxx-mediated H3.3 incorporation [RNA-seq_res]

city: Planegg-Martinsried

first: Gunnar

last: Schotta

address: Grosshaderner Strasse 9

department: Biomedical Center

country: Germany

institute: LMU Munich

summary: Endogenous retroviruses (ERVs) comprise a significant portion of mammalian genomes. Although, specific ERV loci feature regulatory roles for host gene expression, most ERV integrations are transcriptionally repressed by Setdb1 mediated H3K9me3 and DNA methylation. However, the protein network which regulates deposition of these chromatin modifications is still incompletely understood. Here, we performed a genome-wide sgRNA screen for genes involved in ERV silencing and identified the GHKL ATPase protein Morc3 as top scoring hit. Morc3 knock-out cells display de-repression, reduced H3K9me3 and increased chromatin accessibility of distinct ERV classes. We found that the GHKL ATPase domain of Morc3 is critical for ERV silencing, since mutants which cannot bind ATP, or which are defective in ATP hydrolysis cannot rescue the Morc3 ko phenotype. Proteomic analysis revealed that Morc3 mutant protein which cannot bind ATP fails to interact with the H3.3 chaperone Daxx. This interaction depends on Morc3 sumoylation, as Daxx lacking the SUMO interaction domain shows reduced association with Morc3. Notably, in Morc3 ko cells, we observed strongly reduced H3.3 on Morc3 binding sites. Thus, our data demonstrate Morc3 as critical regulator of Daxx-mediated H3.3 incorporation into ERV regions.

overall_design: Transcriptional analysis of wild type and Morc3 rescue mouse embryonic stem cells

first: Sophia

last: Groh


title: Quantitative analysis of transcriptomes from WT and HVCN1-/- 293T cells.

city: Hangzhou

first: Fan

last: Wang

state: Zhejiang

address: Yuhangtang Road 866

institute: Zhejiang University

summary: Our previous data showed that knockout of HVCN1 promotes cell migration in vitro, the results of RNA-Seq indicated that up-regulation of cell migration related genes may be related to it.

overall_design: mRNA profiles of WT and HVCN1-/- 293T cells, 3 replications per group.

first: Jingwei


title: scRNAseq analysis of mouse  L4  whole dorsal root ganglions following sciatic nerve cush, dorsal root crush and spinal cord injury

status: Public on Sep 12 2021

city: Athens

first: Oshri

last: Avraham

state: GA

address: 120 Cedar St

department: Cellular Biology

institute: University of Georgia

summary: After an injury in the adult mammalian central nervous system, lesioned axons fail to regenerate. This failure to regenerate contrasts with the remarkable potential of axons to grow following an injury in the peripheral nervous system. Peripheral sensory neurons with cell soma in dorsal root ganglia (DRG) switch to a regenerative state after nerve injury to enable axon regeneration and functional recovery. Decades of research have focused on the signaling pathways elicited by injury in sensory neurons and in Schwann cells that insulate axons as central mechanisms regulating nerve repair. However, neuronal microenvironment is far more complex and is composed of multiple cell types including endothelial, immune and glial cells. Whether the microenvironment surrounding neuronal soma contribute to the poor regenerative outcomes following central injuries remains largely unexplored. To answer this question, we performed a single cell transcriptional profiling of the DRG neuronal microenvironment response to peripheral and central injuries. In dissecting the roles of the microenvironment contribution, we have focused on a poorly studied glia population of Satellite Glial Cells (SGC) surrounding the neuronal cell soma. Upon a peripheral injury, SGC contribute to axon regeneration via Fatty acid synthase (Fasn)-PPARα signaling pathway. Our analysis reveals that in response to central injuries, SGC do not activate the PPAR signaling pathway. However, induction of this pathway with fenofibrate, an FDA- approved PPARα agonist used for dyslipidemia treatment, rescued axon regeneration following an injury to the central nerves. Collectively, our results uncovered a previously unappreciated role of the neuronal microenvironment differential response in central and peripheral injuries.

overall_design: We have applied the high-throughput single-cell mRNA sequencing technique, using the Chromium Single Cell Gene Expression Solution (10x Genomics) to mouse L4 DRG in naïve and injured conditions (3 days post sciatic nerve crush injury, dorsal root crush or spinal cord injury), n=2 biological samples (NAI,DRC,SCI) n=1 (SNC)

first: Valeria

last: Cavalli


title: Morc3 silences endogenous retroviruses by enabling Daxx-mediated H3.3 incorporation [RNA-seq_wt/ko]

overall_design: Transcriptional analysis of wild type and Morc3 knock out mouse embryonic stem cells


title: Plexin-B2 regulates mechanotension during multicellular organization

city: New York

first: Aarthi

last: Ramakrishnan

state: New York

address: 1425 Madison Avenue

department: Neuroscience

institute: Icahn School of Medicine at Mount Sinai

summary: During multicellular organization, individual cells need to constantly adjust intracellular contractility and junctional adhesive properties in order to maintain tissue cohesion and mechanotension. The membrane receptors linking external biochemical cues and internal cell mechanics are incompletely understood. Here, we reveal that the axon guidance receptor Plexin-B2 regulates intracellular mechanotension, and this in turn impacts cell-cell/cell-matrix adhesiveness during self-assembly of human embryonic stem cells (hESCs) and neuroprogenitor cells (hNPCs) into epithelial structures. The altered tissue mechanics caused by Plexin-B2 deficiency or over expression affects stem cell behaviors as well as β-catenin and YAP mechanosensing. Strikingly, Plexin-B2 deficiency results in accelerated neuronal differentiation, while proper levels of Plexin-B2 activity are required for maintaining cytoarchitectural integrity of the neuroepithelium as modeled in cerebral organoids. Mechanistically, Plexin-B2 engages its extracellular and Ras-GAP domains for mechanoregulation via RAP1/2. Our studies establish mechanoregulation as a key function of Plexin-B2 during multicellular organization, thereby solidifying the principle of force- mediated regulation of stem cell biology and tissue morphogenesis.

overall_design: RNA-sequencing of hESC colonies of WT, PLXNB2 KO, and PLXNB2 OE condition, with three independent replicates for each condition.

first: Chrystian

last: Junqueira Alves

first: Sangjo

last: Kang

first: Theodore

last: Hannah

first: Roland

middle: H

last: Friedel

first: Hongyan

last: Zou


title: Morc3 silences endogenous retroviruses by enabling Daxx-mediated H3.3 incorporation [ChIP-seq]

overall_design: ChIP analysis of the H3K4me3, H3K9me3 and H3K27ac histone modifications, H3.3 histone variant, Setdb1 and wild type and mutant Morc3 in different mouse embryonic stem cell lines

first: Gustavo

middle: P

last: de Almeida


title: Transcriptomic analysis of corticosteroids-treated hiPSC-derived RPE cells

status: Public on Sep 06 2021

city: Paris

first: Min

last: ZHAO

state: France

address: 15 rue de l'Ecole de Médecine

institute: INSERM U1138, Centre de Recherche des Cordelier, University Paris Descartes

summary: The aim of this study was to analyze the pan-transcriptional regulations induced in hiPSC-derived RPE (iRPE) cells by corticoids with specific inhibitors of their receptors to decipher specific genes regulated by MR or GR activation. Cells were seeded at P3 in cell culture plastic dishes. On day 35, one week prior to corticosteroids treatments, RDMw/oA medium was remove and iRPE cells were incubated in experimental corticosteroid-free medium (DMEM, high glucose, HEPES, no phenol red, 10% Fetal Bovine Serum, charcoal stripped). On day 42, iRPE cells were treated for 24 h with the following corticosteroids treatments: aldosterone (10-7 M), cortisol (10-7 M) and cortisol (10-7 M) plus RU-486 (10-5 M).  As corticosteroids were dissolved in ethanol (EtOH) or methanol (MeOH) control cells were treated with 0.1% EtOH or MeOH  in medium. Total RNA samples extracted from iRPE were sequenced at the iGenSeq transcriptomic platform of the Brain and Spine Institute (ICM, Paris, France). RNA quality was checked by capillary electrophoresis (Agilent 2100 Bioanalyzer system) and RNA with integrity numbers (RIN) ranging from 7.8 to 8.2 was accepted for library generation. Quality of raw data has been evaluated with FastQC. Librairies were prepared with Roche KAPA mRNA HyperPrep kit and sequenced with the Illumina NextSeq 500 Sequencing system using NextSeq 500 High Output Kit v2 (150 cycles), 400 millions of reads, 50Gbases. Star v2.5.3a has been used to align reads on reference genome hg19 using standard options. Quantification of gene and isoform abundances has been done with rsem   1.2.28, prior to normalization on library size with edgeR bioconductor package. Finally, differential analysis has been also conducted with edgeR. Multiple hypothesis adjusted p-values were calculated with the Benjamini-Hochberg procedure to control FDR. We identified genes differentially regulated by MR and GR, and those regulated by both MR and GR activation in hiPSC-RPE cells.

overall_design: mRNA profiles of corticosteroids-treated hiPSC-RPE cells

first: Jérémie

last: Canonica

first: Justine

last: Guegan


title: Cold Exposure Protects from Neuroinflammation through Immunologic Reprogramming

status: Public on Sep 04 2021

city: Genève

first: Noushin

last: Hadadi

address: 1 rue Michel-Servet

department: Physiology and Cellular Metabolism

country: Switzerland

institute: University of Geneva

summary: Effects of cold exposure on blood monocytes and spinal cord under EAE were studied

overall_design: mRNA profiles of tissue monoycets and spinal cord under EAE of WT male 8 weeks old C57BL/6J mice

first: Martina

last: Spiljar

first: Karin

last: Steinbach


title: Joint single-cell multiomic analysis identifies Aebp2 as a key regulator in Wnt3a induced asymmetric stem cell division

status: Public on Sep 05 2021

first: Dong

last: Fang

address: 866 Yuhangtang Road

department: Life Sciences Institute

summary: Wnt signal usually functions as a spatial gradient. A localized Wnt3a can induce asymmetric division of mouse embryonic stem cells, whereas proximal daughter cells maintain self-renew and distal daughter cells acquire hallmarks of differentiation. Here, we develop an approach, SET-seq (same cell epigenome and transcriptome sequencing), to jointly profile epigenome and transcriptome in the same single cell. By utilizing SET-seq, we profile H3K27me3 and H3K4me3 with gene expression in Wnt3a induced asymmetric cell division. H3K27me3, but not H3K4me3, is correlatedly changed with gene expression. Single cells clustered by H3K27me3 recapitulate the clusters defined by gene expression. Furthermore, Aebp2, which is the regulator of H3K27me3, is important for the cell-fate decision with localized Wnt signal. Our results provide a convenient way to jointly profile epigenome and transcriptome in the same cell, and uncover the mechanistic insights into the gene regulatory programs for maintaining and resetting stem cell fate during differentiation.

overall_design: Single-cell level epigenomic and transcriptional profile in asymmetric division mESCs

first: Zhongxing

last: Sun

first: Yin

last: Tang

first: Yanjun

last: Zhang

first: Yuan

first: Junqi

last: Jia

first: Weiwu

last: Zeng


title: Transcriptomic analysis of Streptomyces coelicolor Cvn8 mutants on ISP2 agar in isolation or in an interaction [2020RNAseqData]

first: Matthew

last: Traxler

first: Bailey

last: Bonet


title: Coupled protein synthesis and ribosome-guided piRNA processing on mRNAs

city: Rochester

first: Xin

last: Li

state: NY

address: 601 Elmwood Ave

department: Biochemistry and Biophysics

institute: University of Rochester

summary: piRNAs can derive from transposable elements (TEs), long non-coding RNAs, or the 3'UTR of mRNAs, the last being the least characterized out of the three piRNA classes. In this study, we systematically defined the regulation, biogenesis and function of the 3'UTR piRNAs that are expressed throughout mouse spermatogenesis. These piRNAs are regulated by A-MYB transcription factors, and their precursors are bifunctional mRNAs which are processed into piRNAs after pioneer rounds of translation. This dataset includes high-throughput sequencing data that have been used in this study.

sample_organism:
Gallus gallus
Mus musculus

platform_organism:
Gallus gallus
Mus musculus

overall_design: High-throughput sequencing data including RNAseq, small RNa-seq, Ribo-seq and Degradome sequencing of mouse and rooster testis. All sequencing data were sequenced on Illumina platform.

middle: Z

first: Yu

first: Jihong

last: Zheng


title: Blood transcriptomics for diagnosis, risk, and treatment monitoring in tuberculosis reveal the evolution and resolution of TB disease: Does one signature capture all?

city: London

first: Anne

last: OGarra

address: 1 Midland Road

country: United Kingdom

institute: Francis Crick Insititue

summary: Characterization of Tuberculosis (TB) progression, diagnosis and treatment response with blood transcriptional RNA-seq analyses. Focus and underlying host immunological response and identification of new signatures for TB early diagnosis and treatment monitoring response.

overall_design: Blood transcriptomics RNA-seq dataset that includes blood RNA samples collected from TB progressors at different time points before they progress to active TB disease and at time of diagnosis before anti-TB treatment (ATT), and also samples from active TB patients from diagnosis before any anti-TB treatmentATT and followed during treatment at regular time points up to one year after treatment initiation.

first: Olivier

last: Tabone

last: O'Garra


title: Integrating whole blood transcriptomic collection procedures into the current anti-doping testing system, including long-term storage and re-testing of anti-doping samples

status: Public on Sep 03 2021

city: Rome

first: Giscard

middle: Humberto Oliveira

last: Lima

address: Piazza Lauro de Bosis, 15

country: Italy

institute: University of Rome Foro Italico

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: small RNA profiling of bovine milk-derived extracellular vesicles isolated via salting-out

city: Beijing

first: Xiao-Hui

last: Tan

address: 8, Xishiku Street, Xicheng District

institute: Peking University First Hospital

type: Non-coding RNA profiling by high throughput sequencing

summary: We established a novel and cost-effective procedure to isolate extracellular vesicles from bovine milk via salting-out. We aimed to obtain the profiling of the small RNAs in these EVs as an important characterization in EV research.

overall_design: Examination of 3 different samples from bovine milk-derived extracellular vesicles isolated via salting-out

first: Rui-Li

last: Guan


title: Gene expression profiling of CD45+CD11b+F4/80high macrophages in MC38 tumor of WT mice injected with DMSO or picrotoxin

status: Public on Sep 02 2021

city: Suita

first: Katsuyuki

last: Shiroguchi

state: Osaka

address: 6-2-3 Furuedai

department: Center for Biosystems Dynamics Research

country: Japan

institute: RIKEN

summary: We characterized tumor-associated macrophages and found a pro-inflammatory signature of those cells in picrotoxin-treated mice compared to those in control mice (DMSO).

overall_design: Examination one hundred of tumor-associated macrophages freshly sorted from tumor of WT mice injected with DMSO or picrotoxin on day 7 after tumor inoculation

first: Baihao

first: Sidonia

last: Faragasan

first: Nozomi

last: Hojo


title: Disordered breathing in Pitt Hopkins syndrome involves disruption of parafacial respiratory neurons and aberrant expression of Nav1.8.

city: Farmington

first: William

last: Flynn

state: CT

address: 10 Discovery Drive

institute: The Jackson Laboratory

summary: Pitt-Hopkins syndrome (PTHS) is a rare autism spectrum-like disorder characterized by intellectual disability, developmental delays and breathing problems involving episodes of hyperventilation followed by apnea. PTHS is caused by functional haploinsufficiency of the gene encoding transcription factor 4 (Tcf4). Despite the severity of this disease, virtually nothing is known regarding mechanisms contributing to PTHS behavioral abnormalities, and candidate therapeutic targets are lacking. Here, we show that a Tcf4 truncation (Tcf4tr/+) mouse model of PTHS recapitulates respiratory phenotypes observed in PTHS patients. The basis of this behavior deficit involves selective loss of putative expiratory parafacial neurons and compromised function of neurons in the retrotrapezoid nucleus that regulate breathing in response to tissue CO2/H+. We also show that central Nav1.8 channels can be targeted pharmacologically to improve respiratory function at the cellular and behavioral levels in Tcf4tr/+ mice, thus establishing Nav1.8 as a high priority target with therapeutic potential in PTHS.

overall_design: Examination of cells from ventral parafacial brain slices from two batches of Tcf4 mice

first: Colin

last: Cleary

first: Shaun

last: James

first: Brady

middle: J

last: Maher

first: Daniel

middle: K

last: Mulkey


title: Integrating whole blood transcriptomic collection procedures into the current anti-doping testing system, including long-term storage and re-testing of anti-doping samples [Short-term]

summary:
Purpose: Recombinant human erythropoietin administration studies involving “omics” approaches have demonstrated a gene-expression signature that could aid detection of blood doping. However, current anti-doping testing does not involve blood collection into tubes with RNA preservative. This study investigated if whole blood in short-term storage could be used for transcriptomic analysis despite lacking RNA preservation.
Methods: Whole blood samples were collected from fourteen male healthy individuals. Short-term storage: whole blood collected into K2EDTA tubes and subjected to short-term (i.e., at 4°C) storage for 6 hours, 12 hours, 24 hours and 48 hours. After storage, blood from K2EDTA tubes were transferred into Tempus™ Blood tubes, and then extracted using Tempus™ Spin RNA Isolation Kit (Life Technologies, Carlsbad, CA, USA). Samples from four subjects of each time point that presented higher RIN value (≥7) were selected for RNA_Seq analysis.
Results: The experiment provided RNA quality and purity for gene expression analysis. Considering 6-hours storage as a reference group, the number of differentially expressed genes were 19, 45 and 70 in comparison to 12, 24 and 48-hours, respectively (which means 0.37, 0.88 and 1.37% of mapped genes). Of the 19 differentially expressed genes in the comparison 6 vs. 12-hours, 9 overlapped with the 45 in the comparison 12 vs. 24-hours. Furthermore, 40 of those 45 overlapped with the 70 differentially expressed in the comparison 6 vs. 48-hours. None of the transcripts described in previous studies (Durussel et al. 2016; Wang, Durussel, et al. 2017) were differently expressed.
Conclusion: RNA quantity, purity and integrity was not significantly compromised from short-term storage in blood storage tubes lacking RNA stabilisation, indicating that transcriptomic/omics analysis could be conducted using anti-doping samples collected without RNA preservation.

overall_design: Blood samples were collected using K2EDTA tubes and stored at 4C for 6, 12, 24 and 48 hours. After short-term storage, blood samples from K2EDTA tubes were transferred into Tempus tube and extracted by using Tempus™ Spin RNA Isolation Kit. The different gene expression between groups was compared.

first: Alexander

last: Kolliari-Turner

first: Fernanda

middle: R

last: Malinsky

first: Fergus

last: Guppy

first: Renan

last: Martin

first: Guan

last: Wang

first: Sven

middle: C

last: Voss

first: Costas

last: Georgakopoulos

first: Paolo

last: Borrione

first: Fabio

last: Pigozzi

first: Yannis

last: Pitsiladis


title: Gene expression profiling of CD45+CD11b+F4/80high macrophages and CD45+TCRbeta+CD8+ T cells in MC38 tumor of WT, muMt-/- or muMt-/- mice implanted with GABA pellet

first: Katsuyuki

last: Shiroguchi

summary: We characterized the tumor-infiltrating macrophages and CD8 T cells, and we found a pro-inflammatory signature of those cells in muMt-/- mice compared to those in WT mice. Furthermore, many target genes of inflammatory cytokines, such as the TNF target genes, highly expressed in muMt-/- mice, were downregulated by exogenous of GABA.

overall_design: Examination one hundred of tumor-infiltrating macrophages and CD8 T cells freshly sorted from tumor of WT, muMt-/- or muMt-/- mice implanted with GABA pellet on day 7 after tumor inoculation

first: Baihao

last: Zhang

first: Sidonia

last: Faragasan


title: Pivotal Roles for Ribonucleases in Streptococcus pneumoniae Pathogenesis

city: Houston

first: Nicholas

last: De Lay

state: Texas

address: 6431 Fannin St

department: Microbiology and Molecular Genetics

institute: University of Texas Health Science Center

summary: RNases perform indispensable functions in regulating gene expression in many bacterial pathogens by processing and/or degrading RNAs. Despite the pivotal role of RNases in regulating bacterial virulence factors, the functions of RNases have not yet been studied in the major human respiratory pathogen Streptococcus pneumoniae (pneumococcus). Here, we sought to determine the impact of two conserved RNases, the endoribonuclease RNase Y and exoribonuclease polynucleotide phosphorylase (PNPase), on the physiology and virulence of S. pneumoniae serotype 2 strain D39. We report that RNase Y and PNPase are essential for pneumococcal pathogenesis as both deletion mutants showed strong attenuation of virulence in murine models of invasive pneumonia. Genome-wide transcriptomic analysis revealed that nearly 200 mRNA transcripts were significantly up-regulated, whereas the abundance of several pneumococcal sRNAs, including the Ccn (CiaR Controlled Noncoding RNA) sRNAs, were altered in the ∆rny mutant relative to the wild-type strain. Additionally, lack of RNase Y resulted in pleiotropic phenotypes that included defects in pneumococcal cell morphology and growth in vitro. In contrast, Dpnp mutants showed no growth defect in vitro, but differentially expressed a total of 40 transcripts including the tryptophan biosynthesis operon genes and numerous 5’-cis-acting regulatory RNAs, a majority of which were previously shown to impact pneumococcal disease progression in mice using the serotype 4 strain TIGR4. Altogether our data suggest that RNase Y exerts a global impact on pneumococcal physiology, while PNPase-mediates virulence phenotypes, likely through sRNA regulation.

overall_design: Characterization of ribonucleases RNase Y and PNPase in Streptococcus pneumoniae D39 using RNA-seq. Wildtype S. pneumoniae strain and its derived rny and pnp mutants were tested in triplicates.

first: Malcolm

middle: E

last: Winkler


title: Replication timing analysis in polyploid cells reveals Rif1 uses multiple mechanisms to promote underreplication in Drosophila.

city: Nashville

first: Jared

last: Nordman

state: TN

address: 465 21st Ave S

department: Biological Sciences

institute: Vanderbilt University

summary: Regulation of DNA replication and copy number are necessary to promote genome stability and maintain cell and tissue function. DNA replication is regulated temporally in a process known as replication timing (RT). Rif1 is key regulator of RT and has a critical function in copy number control in polyploid cells. In a previous study (Munden et al., 2018), we demonstrated that Rif1 functions with SUUR to inhibit replication fork progression and promote underreplication of specific genomic regions. How Rif1-dependent control of RT factors into its ability to promote underreplication is unknown. By applying a computational approach to measure RT in Drosophila polyploid cells, we show that SUUR and Rif1 have differential roles in controlling underreplication and RT. Our findings reveal that Rif1 functions both upstream and downstream of SUUR to promote underreplication. Our work provides new mechanistic insight into the process of underreplication and its links to RT.

overall_design: Replication timing profiles prepared in salivary gland from female 3rd instar larvae prior to wandering and in fat body from female larvae 96 hours after egg laying (AEL).

first: Souradip

last: Das

first: Madison

last: Caballero

first: Tatyana

last: Kolesnikova

first: Igor

last: Zhimulev

first: Amnon

last: Koren

middle: T


title: Investigating Ngn3-expressing cells in the adult mouse pancreas

first: Rocio

last: Sancho

address: Floor 28 Guy's Hospital

department: Centre for Stem Cells and Regenerative Medicine

institute: King's College London

summary: The beta cell mass of the adult pancreas is thought to be maintained through low-level proliferation. Ductal cells have been proposed as an alternative source of beta cells in vivo, but this remains controversial. By performing detailed lineage tracing analysis, 3D imaging and single cell RNA sequencing we investigated if ductal cells contribute to the beta cell mouse in the adult mouse.

overall_design: Islets isolated from 6 mice of the genotype Ngn3-CreERT: R26-CAG-TdTomato (10 days post-tamoxifen) were dissociated to single cells and analysed using 10X chromium system.

first: Christopher

last: Gribben

last: Lambert

first: Hendrik

last: Messal

first: Chloe

last: Rackham

first: Ella-Louise

last: Hubber

first: Jorge

last: Ferrer

first: Harry

last: Heimberg

first: Peter

last: Jones

first: Axel

last: Behrens


title: An siRNA-guided AGO protein recruits Polymerase V to initiate RNA-directed DNA methylation (smallRNA-seq dataset)

city: St. Louis

first: R. Keith

last: Slotkin

state: Missouri

address: 975 North Warson Road

institute: Donald Danforth Plant Science Center

summary: Foreign DNA is silenced in plants by small RNA-directed DNA methylation (RdDM). RNA Polymerase V (Pol V) is the key protein required to recruit DNA methyltransferases to a RdDM target region. However, the mechanism required for the initial recruitment of Pol V to a targeted locus remains a mystery. In this study, we used first generation (T1) transgene transformations to elucidate a novel mechanism by which Pol V is recruited to both new transgenic and endogenous loci. This study is heavily dependent on analyzing the DNA methylation pattern and small RNAs produced from specific loci. All small RNA sequences (sRNA-seq) and bisulfite converted amplicon sequencing data (BSAS) used in this study are submitted as part of this data series.

overall_design: Examination of small RNA accumulation in wild-type Columbia or mutant plants transformed with specific transgenes.

first: Kaushik

last: Panda

first: Andrea

last: McCue

first: R


title: An siRNA-guided AGO protein recruits Polymerase V to initiate RNA-directed DNA methylation (BSA-seq dataset)

type: Methylation profiling by high throughput sequencing

overall_design: Examination of DNA methylation of specific loci in wild-type Columbia or mutant plants with or without transformation of specific transgenes. Each sequenced library contains amplicons for all the loci investigated in the corresponding genomic background including an unmethylated control locus AT2G20610. See manuscript for the primers used to generate these amplicons.

first: Meredith

last: Sigman


title: CRAC channel controls the differentiation of pathogenic B cells in lupus nephritis

status: Public on Sep 01 2021

city: Guangzhou

first: Binfeng

last: Chen

address: 58 Zhongshan Second Road

institute: Department of Rheumatology, The First Affiliated Hospital, Sun Yat-sen University

summary: Systemic lupus erythematous (SLE) is a prototype of autoimmune disease. Lupus nephritis (LN) is one of the most serious complications of SLE. The development of autoreactive B cells and the production of autoantibodies have been critical for the initiation and progression of LN.   Store-operated Ca2+ entry (SOCE) is the main Ca2+ influx pathway in lymphocytes and is essential for immune response . SOCE is mediated by Ca2+ release-activated Ca2+ (CRAC) channels which are comprised of stromal interaction molecule (STIM) and calcium release-activated calcium modulators (ORAI) . Mutations in genes encoding the CRAC channel abolish SOCE in cells of the immune system and cause severe combined immunodeficiency . Calcium signaling via ORAI1 has been involved in the pathogenesis of autoimmune diseases by driving Th17 differentiation . STIM1 deficiency significantly reduced Th1/Th17 responses and resulted in complete protection from experimental autoimmune encephalomyelitis . Compared to T cells, the roles of CRAC channel in B cells is far less clear.   Ca²⁺/calmodulin (CaM)-dependent protein kinase2 (CaMK2) is a serine/threonine-specific protein kinase that is regulated by the Ca²⁺/CaM complex. CaMK2 has been involved in many signaling pathways and is necessary for Ca²⁺ homeostasis, T cell development and activation. CaMK4, another member of the CaMK family, has been shown to compromises podocyte function and promote renal diseases in LN.   In the current study, we found that CRAC channel mediated calcium signaling is enhanced in B cells from patients with LN. CRAC channel inhibition by YM-58483 and knocked down of CRAC channel by ORAI1 or STIM2 siRNA led to suppression of CaMK2 signaling and decreased B cell differentiation. Lupus mice treated with CRAC channel inhibitor showed reduced anti-double stranded DNA antibodies (anti-dsDNA), decreased immune deposition in the glomeruli and improved renal function. CRAC channel mediates the development and progression of LN by promoting the differentiation of B cells into plasma cells.

overall_design: Naïve human B cells were isolated from 3 donors and stimulated with anti-human IgM (5μg/ml) and anti-human CD40 (1μg/ml) antibodies in the presence of YM-58483 or vehicle for 72h. RNA purification was performed using Qiagen RNeasy Kit (Valencia, CA) and DNA was removed by DNase digestion. RNA quality was defined by RIN and OD260/280. The RNA-seq libraries were made with the Ovation® Ultralow Library Systems and sequenced on an Illumina HiSeq at POHC@IGB. Human reference genome (hg38) was used for alignment using HISAT2. Aligned reads were mapped to known genes. The samples were compared in terms of their total reads mapped to genes; distribution of reads across genes; and global correlation with each other.  50 pg of total RNA was used as input for the SMART-seq v3 cDNA synthesis kit (Takara) using 10 cycles of PCR amplification. 1 ng of cDNA was used as input for the NexteraXT kit (Illumina) using 9 cycles of PCR amplification. Final libraries were quantitated by qPCR and sized distribution determined by Bioanalyzer prior to pooling and sequencing on a HiSeq2500 using 50bp PE chemistry.

first: Xue

last: Li

first: Qin

last: Zeng

first: Shuyi

last: Wang

first: Hui

last: Zhang

first: Niansheng

last: Yang

first: Mengyuan

first: Xionghui

first: Yuefang

last: Huang

first: Mianjing

last: Zhou

first: Yimei

last: Lai

first: Chaohuan

last: Guo

first: Siyuan

last: Zhao


title: Diverse gene expression of diencephalon astrocytes reveals proliferation regulated by Smad4 - scRNA-seq II

city: Neuherberg

first: Pawel

last: Smialowski

address: Ingolstädter Landstraße 1

institute: Helmholtz Zentrum Muenchen

summary: Astrocytes are crucial for neural network function throughout the brain and also show region-specific gene expression differences. To explore this at the single cell level, we isolated cells by ACSA2 MACS from the diencephalon. Single cell RNA-seq revealed two super clusters of cells expressing astrocyte markers, one of which expressed many ependymal markers. Fluorescent labelling of ependymal cells allowed removing them during dissection. The remaining astrocytes and astrocyte-like cells show considerable heterogeneity with some subsets or gene expression states showing more wide-spread and others more restricted mapping of gene expression throughout the forebrain. Surprisingly, diencephalic astrocytes express proliferation regulating genes. Immunostaining for proiliferation markers, DNA-base incorporation and clonal analysis revealed ongoing low level astrocytogenesis even in 8 months old mice. Comparing gene expression of astrocytes in diencephalon and cortex grey matter identified Smad4 as a key regulator of astrocyte in vivo proliferation and in vitro neurosphere formation. Thus, astrocyte diversity is seemingly partitioned in wide-spread and region-specific subsets and reveals the novel concept of adult astrocytogenesis in the diencephalon in a Smad4-dependent manner.

overall_design: Diencephalic astrocytes from 3 months old Aldh1l1-eGFP mice were ACSA2 MACS sorted and processed using Single Cell Reagent Kits V2 from 10x Genomics (scRNA-seq).

first: S

last: Ohlig

first: M

last: Götz

first: P

last: Clavreul

first: J

last: Fischer- Sternjak

first: T

last: Simon-Ebert


title: An siRNA-guided AGO protein recruits Polymerase V to initiate RNA-directed DNA methylation

first: R. Keith

last: Slotkin


title: Mechanistic dissection of dominant AIRE mutations in mouse models reveals AIRE auto-regulation [ChIP-Seq]

city: Rehovot

first: Jakub

last: Abramson

address: 234 Herzl st.

department: Department of Immunology

country: Israel

institute: Weizmann Institute of Science

summary:
Using mouse models of several recessive and putative dominant-negative patient mutations we were able to dissect the mechanisms that underlie the recessive and dominant-negative capacities of the corresponding AIRE mutants, including a newly identified dominant-negative variant C446G
We also identify an auto-regulatory mechanism by which AIRE negatively modulates its own expression.

overall_design: ChIPseq profiles of AIRE binding in sorted mature medullary thymic epithelial cells (mTEChi) from young (4-7 weeks old) Aire +/+, Aire +/C313Y and Aire +/C442G mice generated in the study.

first: Abramson

last: Jakub

first: Goldfarb

last: Yael


title: De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [ATAC-seq]

city: Cambridge

first: Irina

last: Mohorianu

address: Puddicombe Way

department: Wellcome-MRC Cambridge Stem Cell Institute

institute: University of Cambridge

summary:
Genome remethylation is essential for mammalian development. Here we examined cell fate in the absence of de novo DNA methyltransferases. We found that embryonic stem (ES) cells deficient for Dnmt3a and Dnmt3b are rapidly eliminated from chimaeras. Pluripotency progression is derailed towards extra-embryonic trophoblast. This aberrant trajectory is propelled by failure to methylate and suppress expression of Ascl2 during formative transition. Ascl2 deletion rescues transition and improves contribution to chimaeric epiblast but mutant cells are progressively lost in later development. These findings indicate that methylation constrains transcriptome trajectories during developmental transitions by silencing potentially disruptive genes.

This submission is ATAC-seq.

overall_design: Genomic DNA was collected from undifferentiated ES cells and formative EpiLCs from Dnmt3a/3b double knockout cells with control

first: Masaki

last: Kinoshita

first: Meng

middle: A

last: Li

first: Michael

last: Barber

first: Sabine

last: Dietmann

first: Austin

last: Smith


title: Mechanistic dissection of dominant AIRE mutations in mouse models reveals evidence for AIRE auto-regulation [RNA-seq]

overall_design: mRNA profiles of mature medullary thymic epithelial cells (mTEChi) from young (4-7 weeks old) of all mutant mice generated in the study, as well as Aire-/-,were generated by deep sequencing, using the MARSseq method.


title: De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [RNA-seq]

summary:
Genome remethylation is essential for mammalian development. Here we examined cell fate in the absence of de novo DNA methyltransferases. We found that embryonic stem (ES) cells deficient for Dnmt3a and Dnmt3b are rapidly eliminated from chimaeras. Pluripotency progression is derailed towards extra-embryonic trophoblast. This aberrant trajectory is propelled by failure to methylate and suppress expression of Ascl2 during formative transition. Ascl2 deletion rescues transition and improves contribution to chimaeric epiblast but mutant cells are progressively lost in later development. These findings indicate that methylation constrains transcriptome trajectories during developmental transitions by silencing potentially disruptive genes.

This submission is RNA-seq.

overall_design: RNA were collected from undifferentiated ES cells and formative EpiLCs from Dnmt3a/3b double knockout cells with control


title: Mechanistic dissection of dominant AIRE mutations in mouse models reveals evidence for AIRE auto-regulation [ATAC-seq]

overall_design: Chromatin accessibility profiles of mature medullary thymic epithelial cells (mTEChi) from young (4-7 weeks old) Aire +/+, Aire +/C313Y and Aire +/C442G mice generated in the study, as well as Aire-/-,were generated by deep sequencing, using the ATACseq method.


title: Proliferation and neural stem cell potential of diencephalic astrocytes revealed by genome-wide expression is SMAd4 dependent – scRNA-seq

summary: Neural stem cells (NSCs) have astroglial hallmarks, while astrocytes in the intact adult mammalian brain parenchyma are thought to be postmitotic and lack NSC hallmarks that are activated only after injury. Analysis of genome-wide expression at population and single cell level in astrocytes from the diencephalon (DIE) and the cerebral cortex Grey grey Matter matter (CTX GM) revealed cell cycle associated gene expression, that we verified in situ by PCNA immunostaining and incorporation of the thymidine analog EdU. Strikingly, clonal analysis using GLASTCreERT2/confetti mice showed that only diencephalic astrocytes give rise to daughter cells in multi-cellular clones. In addition, subsets of astrocytes only from the diencephalon form multipotent, self-renewing neurospheres in vitro. Given the differential expression levels of genes related to Smad mediated transcriptional regulation between CTX GM and DIE astrocytes, we deleted the common mediator Smad4 in adult astrocytes. This abrogates proliferation of diencephalic astrocytes in vivo and their neurosphere formation in vitro. This work therefore identified a novel astrocyte subtype with NSC hallmarks in the diencephalon and implicates ongoing astrocytogenesis as a region-specific hallmark in the adult brain.

overall_design: Diencephalic astrocytes from 3 months old Aldh1l1-eGFP mice were ACSA2 MACS sorted and processed using Single Cell 3’ Reagent Kits V2 from 10x Genomics (scRNA-seq).

first: Stefanie

first: Magdalena

first: Solène

first: Judith

first: Tatiana


title: Proliferation and neural stem cell potential of diencephalic astrocytes revealed by genome-wide expression is SMAd4 dependent – RNAseq

first: Pawel

overall_design: Whole genome RNA-Seq analysis of translated mRNA in astrocytes from diencephalon and cortical grey matter of Ribotag * GlastCreERT2 * Rpl22HH adult mice of both sexes.

first: Nirmal

last: Kannayian

first: Moritz

last: Rossner

first: Manja

last: Thorwirth


title: Proliferation and neural stem cell potential of diencephalic astrocytes revealed by genome-wide expression is SMAd4 dependent

last: Smialowski

overall_design: Refer to individual Series


title: Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements [ChIP-Seq]

status: Public on Aug 31 2021

city: shanghai

first: yijing

last: zhang

address: 2005 Songhu Road

department: Biochemistry

institute: Fudan University

summary: The yield of wheat is highly impacted by environmental stresses. The combinatorial regulation of sequence-specific transcription factors(TFs) defines a regulatory network that underlies plant stress responses. Here we created a comprehensive catalog of genomic binding sites of 115 TFs underlying abiotic stress responses by leveraging DAP-seq in Triticum Urartu, along with epigenomic profiles. The majority of gene distant TF binding sites(TFBS) are embedded in transposable elements(TEs), whose functional relevance was supported by a signature of purifying selection and active epigenomic features. Furthermore, ~30% non-TE TFBS share high sequence similarity with TE-embeded TFBS, potentially derived from Triticeae-specific TEs and have almost no sequence homology in non-Triticeae species. The expansion of TE-derived TFBS in wheat linked to wheat-specific stress responsive genes, suggesting that TEs are an important driving force for regulatory innovation. Altogether, TEs have significantly and continuously shaped regulatory network in wheat adaptation.

overall_design: In order to delineate the major TF regulatory circuitry to abiotic stresses in Triticum Urartu, we  performed DAP-seq to obtain a genome-wide binding profile of  stress response TFs,  ChIP-seq for three well-studied histone modifications (including H3K9ac, H3K4me3 and H3K27me3), DNase-seq, Bisulphite-seq and RNA-seq in 5 stresses.

first: Yijing

last: Zhang


title: Transcriptional Control of Brain Tumour Stem Cells by a Carbohydrate Binding Protein

city: Ottawa

first: Arezu

last: Jahani-Asl

state: Ontario

address: 451 Smyth Road

department: Department of Cellular and Molecular Medicine

country: Canada

institute: University of Ottawa

summary: Brain tumour stem cells (BTSCs) and intratumoural heterogeneity represent major challenges in glioblastoma therapy. Here, we report that the LGALS1 gene, encoding the carbohydrate binding protein, galectin1, is a key regulator of BTSCs and glioblastoma resistance to therapy. Genetic deletion of LGALS1 alters BTSC gene expression profiles and results in downregulation of gene sets associated with mesenchymal subtype of glioblastoma. Using a combination of pharmacological and genetic approaches, we establish that inhibition of LGALS1 signalling in BTSCs impairs self-renewal, suppresses tumourigenesis, prolongs lifespan, and improves glioblastoma response to ionizing radiation in preclinical animal models. Mechanistically, we show that LGALS1 is a direct transcriptional target of STAT3 with its expression robustly regulated by the ligand OSM. Importantly, we establish that galectin1 forms a complex with the transcription factor HOXA5 to reprogram BTSC transcriptional landscape. Our data unravel an oncogenic signalling pathway by which galectin1/HOXA5 complex maintains BTSCs and promotes glioblastoma.

overall_design: Identification of LGALS1 target genes in brain tumour stem cell, three LGALS1 KO and three control samples.

first: Hamed

middle: S

last: Najafabadi

first: Ahmad

last: Sharanek

first: Aldo

last: Hernandez-Corchado


title: Vaccine driven lung TRM cells provide immunity against Klebsiella via fibroblast IL-17R signaling

city: New Orleans

first: Jay

last: Kolls

state: LA

address: 1430 Tulane Ave

department: Medicine

institute: Tulane University

summary: Subunit vaccine elicits lung tissue resident memmory CD4+ T-cells and confers lung protection against heterologous strain

overall_design: I. We harvested the lungs from Il17raDermoCre negative and positive mice at 4 hours post challenge with 10^4 CFU K1 strain (KP396) and extracted the whole RNAs. We chose this time point based on the similar CFU between groups because any differences in gene expression would not be due to lung bacterial burdens.

first: Naoki

last: Iwanaga


title: Inherited human c-REL deficiency disrupts adaptive immunity

city: MONTREAL

first: David

last: Langlais

state: QC

address: 740 Ave Dr Penfield, rm 4203, McGill Genome Centre

department: Human Genetics

institute: McGill University

summary: Various inborn errors of the canonical NF-kB pathway underlie different forms of human immunodeficiency. However, no patients with autosomal recessive complete deficiencies of RelA, c-REL, or NF-kB1, the three core members of the canonical NF-kB pathway, have yet been identified. We report a child homozygous for a loss-of-expression mutation of REL, encoding c-REL, which is expressed principally in myeloid and lymphoid cells. The distribution of myeloid subsets is normal in this patient, but in vitro-derived monocytes and cDC1s, unlike cDC2s, have impaired IL-12 and IL-23 production. The patient has low frequencies of memory CD4+ T cells, Th1*, Th2, Tregs, and almost no memory B cells. The frequencies of the other lymphoid subsets are normal. The patient’s naïve and memory CD4+ T cells produce only small amounts of IL-2, and the addition of this interleukin rescues their proliferation in response to mitogens, but not to antigens, in vitro. However, we found that HLA-syngeneic control cDCs rescued the proliferation of these cells in response to recall antigens. The production of key effector cytokines, such as IL-4, IL-17A, and IFNg, by memory CD4+ T cells was also highly impaired ex vivo, as was the differentiation of naïve CD4+ T cells into Th1 and Th17 cells in vitro. Both the survival and proliferation of the patient’s naïve B cells were found to be compromised, preventing B-cell differentiation into immunoglobulin (Ig)-secreting plasmablasts in vitro. As a consequence of this pleiotropic effect, this child suffered from severe viral, mycobacterial, fungal, and parasitic infections, while IgG substitution treatment prevented pyogenic infections. The immunological and infectious phenotypes were of hematopoietic origin, as they were cured by hematopoietic stem cell transplantation. Inherited human c-REL deficiency impairs multiple core functions of DCs, T cells, and B cells, thereby disrupting adaptive immunity to multiple infections.

overall_design: Given the patient T and B cell phenotype, we sought to identify the genomic regions bound by c-Rel in naive B and CD4 T cells, as well as in EBV cells.

first: Romain

last: Lévy

first: Jean-Laurent

last: Casanova

first: Mehdi

last: Emam


title: Two Distinct Sertoli Cell States are Regulated via Germ Cell Crosstalk [scRNA-seq]

city: Pullman

first: Michael

last: Griswold

state: WA

address: Biotechnology Life Sciences

department: School of Molecular Biosciences; Center for Reproductive Biology

institute: Washington State University

summary: We report single-cell RNA-sequencing data for RFPxAMH-Cre sorted Sertoli cells from unsynchronized adult testes.

overall_design: Sertoli cells from RFPxAMH-Cre adult testes were isolated and processed for single-cell RNA-sequencing analysis using the 10X Genomics system.

first: Rachel

last: Gewiss

first: Nathan

last: Law

first: Aileen

last: Helsel

first: Erich

last: Shelden


title: Two Distinct Sertoli Cell States are Regulated via Germ Cell Crosstalk

summary: We report bulk RNA-sequencing for synchronized adult Sertoli cells in germ cell-sufficient (RFPxAMH-Cre) and germ cell-deficient (NANOS2 KO) mice.  We also have single-cell RNA-sequencing data for RFPxAMH-Cre sorted Sertoli cells from unsynchronized adult testes (not included in this series).

overall_design: Transcriptional profiling of Sertoli cells in germ cell-sufficient and germ cell-deficient environments.  RFPxAMH-Cre cells were synchronized and sorted to obtain Sertoli-enriched populations and were clustered into 5 categories based on the most enriched stages:  Group A (Stages XI-XII), Group B (Stages I-III), Group C (Stages IV-VI), Group D (Stages VII-VIII), and Group E (IX-X).  NANOS2 KO cells were synchronized and euthanized between 42-50 days post-RA injection to encompass the timing of a full cycle of the seminiferous epithelium.


title: Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements [DAP-Seq]

first: yijing

last: zhang

overall_design: In order to delineate the major TF regulatory circuitry to abiotic stresses in Triticum Urartu, we performed DAP-seq to obtain a genome-wide binding profile of stress response TFs, ChIP-seq for three well-studied histone modifications (including H3K9ac, H3K4me3 and H3K27me3), DNase-seq, Bisulphite-seq and RNA-seq in 5 stresses.


title: Disabling de novo DNA methylation in embryonic stem cells allows an illegitimate fate trajectory

first: Irina

last: Mohorianu

summary:
Genome remethylation is essential for mammalian development but specific reasons are unclear. Here we examined embryonic stem (ES) cell fate in the absence of de novo DNA methyltransferases. We observed that ES cells deficient for both Dnmt3a and Dnmt3b are rapidly eliminated from chimeras. On further investigation we found that in vivo and in vitro the formative pluripotency transition is derailed toward production of trophoblast. This aberrant trajectory is associated with failure to suppress activation of Ascl2. Ascl2 encodes a bHLH transcription factor expressed in the placenta. Misexpression of Ascl2 in ES cells provokes transdifferentiation to trophoblast-like cells. Conversely, Ascl2 deletion rescues formative transition of Dnmt3a/b mutants and improves contribution to chimeric epiblast. Thus, de novo DNA methylation safeguards against ectopic activation of Ascl2. However, Dnmt3a/b-deficient cells remain defective in ongoing embryogenesis. We surmise that multiple developmental transitions may be secured by DNA methylation silencing potentially disruptive genes.

This SuperSeries is composed of the SubSeries listed below.


title: Rational biomarker development for the early and minimally invasive monitoring of AML

city: Memphis

first: Sherif

last: Abdelhamed

address: 262 Danny Thomas Place

department: Pathology

institute: St Jude Children's Research Hospital

summary: We investigated circulating plasma EVs miRNA from 12 AML patients versus 12 healthy donors to identify a miRNA signature as a potential  biomarker for patients with AML.

overall_design: Plasma samples were collected from patients or healthy donors, EVs were isolated by serial high-speed centrifugation, total RNA was extracted and used used to generate cDNA libraries and perform a next-generation sequencing using NextSeq500.

first: John

last: Butler

first: Seul

last: Jung

first: Ding-Wen

last: Chen

first: Gaye

last: Jenkins

first: Lina

last: Gao

first: Jeong

middle: Y

last: Lim

first: Jeffery

last: Klco

first: Terzah

last: Horton

first: Peter

last: Kurre


title: Progressive Decline of Function in Renal Allografts with Normal One Year Biopsies

city: Rochester

first: Walter

last: Park

state: MN

address: 200 1st ST SW

institute: Mayo Clinic

summary: Histologic findings on 1-year biopsies such as inflammation with fibrosis and transplant glomerulopathy predict renal allograft loss by 5 years.  However, almost half of the patients with graft loss have a 1-year biopsy that is either normal or has only interstitial fibrosis.  The goal of this study was to determine if there was a gene expression profile in these relatively normal 1-year biopsies that predicted subsequent decline in renal function. Using transcriptome microarrays we measured intragraft mRNA levels in a retrospective Discovery cohort (170 patients with a normal/minimal fibrosis 1-year biopsy, 54 with progressive decline in function/graft loss and 116 with stable function) and developed a nested 10-fold cross-validated gene classifier that predicted progressive decline in renal function (positive predictive value=38±34%%; negative predictive value=73±30%, c-statistic=0.59).  In a prospective, multicenter Validation cohort (270 patients with Normal/Interstitial Fibrosis [IF]), the classifier had a 20% positive predictive value, 85% negative predictive value and 0.58 c-statistic. Importantly, the majority of patients with graft loss in the prospective study had 1-year biopsies scored as Normal or IF.  We conclude predicting graft loss in many renal allograft recipients (i.e. those with a relatively normal 1-year biopsy and eGFR >40) remains difficult.

overall_design: RNA from 1 year renal allograft surveillance biopsies considered normal/fibrosis that had a subsequent clinical phenotype of stable (Non-Progressor) or progressive decline in 1-5 year renal function (Progressor).

first: Byron

last: Smith

first: Mark

last: Stegall


title: Characterizing Macrophage Diversity in Metastasis-Bearing Lungs Reveals a Lipid-Associated Macrophage Subset

city: Minneapolis

first: Rebecca

last: LaRue

address: 117 Pleasant St SE

department: Department of Lab medicine and Pathology

institute: University of Minnesota

summary: Single cell RNA sequencing was performed on CD45+Ly6G-CD64+MerTK+ macrophages isolated from the lungs of mice 5 weeks after transplantation of 4T1-Luc mammary gland tumors. The purpose of this study was to determine the unique macrophage subsets present in the lungs of mice bearing mammary tumor metastases.

overall_design: Mice received injections of 10k 4T1-Luc cells into the #4 mammary gland. Tumors were allowed to progress for 5 weeks, at which point the lungs were harvested. The lungs were digested and macrophages were sorted by FACS, followed by single cell RNA sequencing.

first: Danielle

middle: N

last: Huggins

first: Ying

last: Wang

first: Todd

last: Knutson

first: Yingzheng

last: Xu

first: Jesse

middle: W

last: Williams

first: Kathryn

middle: L

last: Schwertfeger


title: Runx2-target molecules in limb bud cells

city: Suita

first: Yoshifumi

last: Takahata

department: Dentistry

institute: Osaka University

summary: To identify novel molecules involved in osteoblastogenesis and bone formation, RNA-seq analyses was performed using limb bud cells infected with Venus control, Runx2 or Bmp2.

overall_design: mRNA profiles of mouse limb bud cells infected with Venus, Runx2 or Bmp2 adenovirus (n=2)

first: Riko

last: Nishimura


title: Gene expression changes in CNS and muscle in barentsz mutants

city: New York

first: Jessica

middle: Esther

last: Treisman

address: SKI 4/9, 540 First Avenue

department: Skirball Institute/Cell Biology

institute: NYU School of Medicine

summary: Barentsz (Btz) encodes a subunit of the exon junction complex (EJC), which is involved in post-transcriptional regulation. We found that Btz has functions in neuromuscular development in the Drosophila larva that are independent of the EJC. To identify the genes that it regulates in this process, we carried out an RNA-seq experiment to compare btz2/Df(3R)BSC497 to control btz2/+ tissues. We examined RNA from dissected central nervous systems and carcasses from third-instar larvae. Among the genes that were affected, we found that dawdle (daw) was down-regulated in both tissues. daw encodes an Activin famiily ligand that regulates neuromuscular synapse growth, and we found that daw overexpression could rescue the synapse growth phenotype of btz mutants.

overall_design: Three biological replicates were analyzed for each tissue (third-instar larval CNS or muscle) in each condition (btz/+ or btz/Df).

first: Cheuk

last: Ho

first: Jean-Yves

last: Roignant

first: Zuojian

last: Tang

first: Stuart

last: Brown


title: Two Distinct Sertoli Cell States are Regulated via Germ Cell Crosstalk.

first: Michael

last: Griswold

summary: This SuperSeries is composed of the SubSeries listed below.


title: STING-driven interferon signaling triggers metabolic alterations in pancreas cancer cells visualized by [18F]FLT PET imaging

status: Public on Aug 30 2021

city: Los Angeles

first: Caius

middle: Gabriel

last: Radu

state: CA

address: 650 Charles E. Young Drive, South

department: Molecular and Medical Pharmacology

institute: University of California Los Angeles

summary: Type I interferons (IFNs) are critical effectors of emerging cancer immunotherapies designed to activate pattern recognition receptors (PRRs). A challenge in the clinical translation of these new immuno-modulatory agents is the lack of pharmacodynamic biomarkers indicative of increased intratumoral IFN signaling following PRR activation. Positron emission tomography (PET) imaging enables the visualization of tissue metabolic activity but whether IFN signaling-induced alterations in tumor cell metabolism can be detected using PET has not been investigated. We found that IFN signaling augments pancreatic ductal adenocarcinoma (PDAC) cell nucleotide metabolism via transcriptional induction of metabolism-associated genes including thymidine phosphorylase (TYMP). TYMP catalyzes the first step in the catabolism of thymidine which competitively inhibits intratumoral accumulation of the nucleoside analog PET probe [18F]-fluorothymidine ([18F]FLT). Accordingly, IFN treatment stimulates cancer cell [18F]FLT uptake in the presence of thymidine and this effect is dependent on TYMP expression. In vivo, genetic activation of stimulator of interferon genes (STING), a PRR widely expressed in PDAC, enhances the [18F]FLT avidity of xenograft tumors. Treatment with a small molecule STING agonist triggers IFN signaling-dependent TYMP expression in PDAC cells and enhances both subcutaneous and orthotopic tumor [18F]FLT uptake in vivo following systemic treatment. These findings indicate that [18F]FLT accumulation in tumors is sensitive to IFN signaling and that [18F]FLT PET may serve as a novel pharmacodynamic biomarker for PRR agonist-based immunotherapies in PDAC and possibly other malignancies characterized by elevated STING expression.

overall_design: Our goal was to define transcriptional alterations triggered by type I IFN (IFNβ) exposure in SUIT2 human pancreas cancer cell cultures following either 6 or 24 hours of treatment.

first: Keke

last: Liang

first: Evan

last: Abt

first: Thuc

middle: M

last: Le

first: Arthur

last: Cho

first: Jing

last: Cui

first: Luyi

last: Li

first: Amanda

last: Dann

first: Khalid

last: Rashid

last: Creech

first: Razmik

last: Ghukasyan

first: Nanping

last: Wu

first: Ethan

last: Rosser

first: Liu

last: Wei

first: Giuseppe

last: Carlucci

first: Johannes

last: Czernin

first: Timothy

last: Donahue

middle: G


title: Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

city: London

first: Caroline

last: Hill

address: 1 Midland Road

department: Developmental Signalling

institute: Francis Crick Institute

summary: We explored the consequence of Smad4 gene loss for gene expression downstream BMP and Nodal signalling. To this end we performed RNA sequencing of WT and MZsmad4a mutants at mid-gastrulation.

overall_design: To capture global transcriptomic changes devoid of inter-embryo variability bias we processed three biological replicates for each genotype.

first: Luca

last: Guglielmi

first: Christopher

last: Barrington


title: Expression data PIK3CA E545K vs PIK3CA H1047R stably transfected in human HCC cell lines

status: Public on Aug 29 2021

city: Regensburg

first: Alexander

last: Scheiter

state: Bavaria

address: Franz-Josef-Strauss Allee 11

department: Institute of Pathology

institute: University of Regensburg

summary:
Human HCC cell lines SNU387 and SNU449 stably transfected (lentivirus) with PIK3CA E545K, PIK3CAH1047R, EGFP or WT.
Comparison to determine differential effectors of PIK3CA helical and kinase domain mutants by microarray.

overall_design: Lysates of the above mentioned stably transfected or wildtype cell lines were generated. No additional treatment was performed.

first: Scheiter

last: Alexander


title: Analysis of Transcriptome in small intestine after radiation injury with treatment of pravastatin

city: Seoul

first: Hyosun

last: Jang

address: Nowongu Nowonro 75

country: South Korea

institute: Korea Institute of Radiological & Medical Science

summary: This study is designed to understand whether Pravastatin (Pra) treatment alters the transcriptome of small intestine after radiation injury. RNA was extracted from 15 Gy abdominal irradiated Gottingen minipigs with PS treatment. A cDNA library was generated using a TruSeq Stranded mRNA sample prep kit (Illumina, San Diego, CA), and transcriptome sequencing was performed using a TruSeq 3000/4000 SBS kit and Illumina sequencer with 101 bp paired-end reads per sample (Macrogen, Seoul, Korea).

overall_design: mRNA profiles of Pra-treated irradiated intestine on Gottingen minipigs were sequenced using Illumina. (2 minipigs of control group, 2 minipigs of irradiation (IR), and 2 minipigs of PS-treated with irradiation (IR+PS))

first: Jang

last: Hyosun

first: Shim

last: Sehwan


title: Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements I

first: yijing

last: zhang

summary: The yield of wheat is highly impacted by environmental stresses. The combinatorial regulation of sequence-specific transcription factors(TFs) defines a regulatory network that underlies plant stress responses. Here we created a comprehensive catalog of genomic binding sites of 115 TFs underlying abiotic stress responses by leveraging DAP-seq in Triticum Urartu, along with epigenomic profiles. The majority of gene distant TF binding sites(TFBS) are embedded in transposable elements(TEs), whose functional relevance was supported by a signature of purifying selection and active epigenomic features. Furthermore, ~30% non-TE TFBS share high sequence similarity with TE-embeded TFBS, potentially derived from Triticeae-specific TEs and have almost no sequence homology in non-Triticeae species. The expansion of TE-derived TFBS in wheat linked to wheat-specific stress responsive genes, suggesting that TEs are an important driving force for regulatory innovation. Altogether, TEs have significantly and continuously shaped regulatory network in wheat adaptation.

first: Yijing

last: Zhang


title: Ssl2/TFIIH Function in Transcription Start Site Scanning by RNA Polymerase II in Saccharomyces cerevisiae

status: Public on Aug 28 2021

city: Pittsburgh

first: Tingting

last: Zhao

state: PA

address: 4200 Fifth Ave

institute: University of Pittsburgh

summary: The initial step of RNA polymerase II (Pol II) transcription involves a large number of transcription factors and arises at multiple sites within most promoters. TFIIH is an essential, multi-subunit transcription factor that assembles on promoter DNA with Pol II and five other general transcription factors (GTFs) to form a pre-initiation complex (PIC) for basal transcription. During transcription initiation, TFIIH melts promoter DNA through the ATPase activity of its Ssl2 subunit. In the model eukaryote Saccharomyces cerevisiae, after DNA melting, Pol II scans downstream for usable transcription start sites (TSSs). To understand the function of Ssl2/TFIIH in promoter scanning and TSS selection, we identified novel alleles of SSL2 in genetic screens for mutants defective in TSS distribution that may potentially arise from altered scanning. Consistent with this notion, these ssl2 alleles alter scanning in ways that are distinct from how changes to the Pol II active site alter scanning and this difference is observed genome-wide. Our investigations support two major pathways in controlling promoter scanning and TSS selection, one controlling the efficiency of initiation through Pol II activity or factors regulating Pol II activity; another network appears to control the processivity of scanning by Ssl2/TFIIH.

overall_design:
We report the application of transcription start site sequencing (TSS-seq) and ChIP-exo in high-throughput profiling of RNA polymerase II (Pol II) transcription start site usage and PIC component positioning in the budding yeast Saccharomyces cerevisiae. We applied TSS-seq on six ssl2/TFIIH mutants that were either previously reported defective in Pol II transcription or from our genetic screening indicating possible TSS usage defects. We also applied TSS-seq on wild-type yeast strains and two Pol II mutant that were previously characterized by us for comparison purposes. ChIP-exo was applied on two ssl2/TFIIH mutant that alter TSS usage in distinct patterns to investigate ssl2/TFIIH’s effects on PIC positioning. Raw data of TSS-seq and ChIP-exo were also deposited in NCBI BioProject, under the accession number PRJNA681384.

The GSM records describe a single biological Sample. Submitter created a bioSample (SAMN) for each R1 and R2 read of that single sample.

first: William

last: Lai

first: Craig

middle: D

last: Kaplan


title: An NSD3-targeting PROTAC (Proteolysis Targeting Chimeric) suppresses the NSD3 and cMyc oncogenic nodes in cancer cells

city: DURHAM

first: Chenxi

last: Xu

state: North Carolina

address: 3 Genome Court

department: Department of Pharmacology and Cancer Biology

institute: Duke university

summary: Nuclear receptor binding SET domain protein 3 (NSD3), a gene located within the 8p11-p12 amplicon frequently detected in human cancers, encodes a chromatin modulator and an attractive onco-target. However, agent that can effectively suppress the NSD3-mediated oncogenic actions is currently lacking. Here, we report an NSD3-targeting proteolysis targeting chimera (PROTAC), termed MS9715, which achieves effective and specific depletion of NSD3 and interacting partners (including cMyc) in tumor cells. We show that MS9715-induced NSD3 degradation relies on BI-9321, an antagonist module binding the PWWP1 domain of NSD3, and VHL, which is chemically conjugated to BI-9321 via a linker and a VHL ligand. Importantly, compared to BI-9321, a recently disclosed NSD3 antagonist, MS9715 is more potent in suppressing growth of the NSD3-dependent hematological cancer including models of MLL-rearranged acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-ALL) and multiple myeloma (MM), and uniquely mediates simultaneous depletion of cellular NSD3 and cMyc. Transcriptome profiling further demonstrates effective actions of MS9715 but not BI-9321 in suppressing both the NSD3- and cMyc-mediated gene-expression programs, a phenomenon reminiscent of the CRISPR/cas9-mediated knockout (KO) of NSD3. Together, this study reports a first-in-class NSD3 degrader suitable for co-suppressing NSD3- and cMyc-related oncogenic nodes in cancer, suggesting a novel therapeutic strategy,

overall_design: Examination of transcriptome profiles in the EOL-1 cells post-treatment with 2.5 μM of either DMSO, BI-9321 (an NSD3 PWWP1 binding inhibitor), MS9715 (a BI-9321- and VHL-dependent PROTAC degrader of NSD3) or MS9715N (an MS9715-related analog compound incapable of binding to VHL E3 ligase).

first: Gang

last: Wang


title: Temporal inhibition of chromatin looping and enhancer accessibility during neuronal remodeling.

city: Buffalo

first: Dahong

last: Chen

state: Other

address: 955 Main Street

institute: SUNY Buffalo

summary: We report the 4C-seq data and ChIP-seq to study Shep regulation of chromatin looping.  We also reported ATAC-seq and CUT&Tag data on sorted neurons that reveal chromatin accessibility and states during the neuronal remodeling of Drosophila melanogaster

overall_design: Examine regulation of chromatin looping, accessibility and states during neuronal remodeling

first: Catherine

last: McManus

first: Behram

last: Radmanesh

first: Leah

last: Matzat

first: Elissa

last: Lei


title: Gene expression profiling in a mouse model of spiral ganglion neuron degeneration

city: Shanghai

first: Quan

state: Shanghai

address: No.197 Ruijin 2nd Road, Shanghai, 200025, China

institute: Shanghai Jiaotong University School of Medicine

summary: The goals of this study are to identify transcripts that participate in the degeneration of spiral ganglion neurons.

overall_design: Gene expression profiles of mice cochlear ganglion neurons in wild type group and degenerated group were generated by deep sequencing, in triplicate, using Illumina Hiseq 2500 platform.

first: Yilin

last: Shen

first: Bin

last: Ye

first: Mingliang

last: Xiang


title: Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (MCC)

city: Headington

first: Damien

last: Downes

state: Oxfordshire

address: John Radcliffe Hospital

department: MRC Weatherall Institute of Medicine

institute: The University of Oxford

summary: To identify regulatory interactions in erythroid, fibroblast and endothelial cells Micro Caputre-C was carried outfrom the promoters of active genes as well as the rs17713054 containing enhancer.

overall_design: MCC was carried out from 12 viewpoints in at least 3 replicates each of H441 lung epithelial cells, IMR-90 liung fibroblast cells, human umbilical vein endothelial cells (HUVEC) and Human Umbilical Derived Erythroid Progenitor line 2 cells (HUDEP-2).

first: Peng

last: Hua

first: James

middle: O

last: Davies

middle: J


title: Identify molecules regulated by glucosylceramide synthase in mouse osteoblasts.

city: Nagoya

first: Kazunori

last: Hamamura

address: 1-100 Kusumoto-cho, Chikusa-ku

department: Pharmacology

institute: Aichi Gakuin University, School of Dentistry

summary: To identify molecules regulated by glucosylceramide synthase in osteoblasts, we conducted microarray analysis using samles treated with the inhibitors of glucosylceramide synthase.

overall_design: Four groups for MC3T3-E1 cells were Control, Miglustat, D-PDMP, and D-PPMP.  The concentrations of Miglustat, D-PDMP, and D-PPMP were 50 microM, 10 microM, and 1.0 microM, respectively.  Four days after treatment of their inhibitors of GCS, the cells were plated at 2.5 x 100000 cells into 60 mm dishes, and cultured for 24 h.  The cells were harvested for microarray analysis.


city: Houston

first: Consuelo

last: Walss-Bass

address: 1941 East Road Rm. 3110

department: Louis A. Faillace Department of Psychiatry and Behavioral Sciences

institute: University of Texas Health Science Center at Houston

summary:
From Stertz et al 2021 "Human-induced pluripotent stem cells (hiPSCs) allow for the establishment of brain cellular models of psychiatric disorders that account for a patient’s genetic background. Here, we conducted an RNA-sequencing profiling study of hiPSC-derived cell lines from schizophrenia (SCZ) subjects, most of which are from a multiplex family, from the population isolate of the Central Valley of Costa Rica. hiPSCs, neural precursor cells, and cortical neurons derived from six healthy controls and seven SCZ subjects were generated using standard methodology. Transcriptome from these cells was obtained using Illumina HiSeq 2500, and differential expression analyses were performed using DESeq2 (|fold change|>1.5 and false discovery rate < 0.3), in patients compared to controls. We identified 454 differentially expressed genes in hiPSC-derived neurons, enriched in pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with serum-glucocorticoid kinase 1 (SGK1), an inhibitor of glycogen synthase kinase 3β, as part of this pathway. We further found that pharmacological inhibition of downstream effectors of the PI3K/GSK3 pathway, SGK1 and GSK3, induced alterations in levels of neurite markers βIII tubulin and fibroblast growth factor 12, with differential effects in patients compared to controls. While demonstrating the utility of hiPSCs derived from multiplex families to identify significant cell-specific gene network alterations in SCZ, these studies support a role for disruption of PI3K/GSK3 signaling as a risk factor for SCZ."
This dataset includes Samples from the manuscript "Convergent genomic and pharmacological evidence of PI3K/GSK3 signaling alterations in neurons from schizophrenia patients"  by Stertz et al 2021 published in Neuropsychopharmacology.

overall_design: In total, raw fastq for 13 Neural Progenitor Cells, 11 Cortical Neurons, 4 pooled induced pluripotent stem cell lines, and 4 pooled lymphoblastoid cell lines are uploaded and have processed counts provided. These counts were used to generate the conclusions in the manuscript.

first: Stertz

last: Laura

first: Pei

last: Guangsheng

first: Zhao

last: Zhongming

first: Walss-Bass

last: Consuelo


title: Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements

city: shanghai

first: yijing

last: zhang

address: 2005 Songhu Road

institute: Fudan University

overall_design: Refer to individual Series


title: Comparative analysis of liver tissues from heahtly mice and mice suffering from cholangitis

city: Paris

first: Pierre

last: de la Grange

address: 29, rue du Faubourg Saint-Jacques

department: Paris Biotech Santé

institute: GenoSplice technology

summary: The goal of the study was to compare the transcriptomic signature (by bulk RNA-sequencing) of hepatic tissues of mice either healthy/normal or affected with primary sclerosing cholangitis (PSC) or primary biliary cholangitis mouse (PBC) (Paillet et al, J Exp Med, 2021). Transcriptomic analyses revealed mostly convergent alterations in the gene expression patterns when PBC and PSC were compared to normal, age- and sex-matched controls. Gene Ontology (GO) term analyses of the modulated mRNAs revealed a significant enrichment of genes involved in inflammation, immune response and chemotaxis of different leukocyte subsets . The expression of genes listed under the GO terms “inflammation” and “neutrophil” was not significantly different (p>0.5, Student t-test) between PBC and PSC. In sharp contrast, genes listed under the GO terms “T cell” and “B cell” were significantly (p<0.05, Student t-test) upregulated in PBC compared to PSC livers. Deeper analysis of the aforementioned liver RNA-seq dataset indicated that several genes specifically involved in Th1 and Tc1 responses were upregulated in PBC livers with respect to controls and, in some cases also with respect to PSC. Especially, this applies to Tc1-related genes encoding the markers CD8a, CD274 (best known as PD-L1), UL16 binding protein 1 (ULBP1), IFNγ, G Protein-Coupled Receptor 18 (GPR18), the transcription factor suppressor of cytokine signaling 1 (SOCS1), and the cytotoxic protease granzyme B (GzmB) (Paillet et al, J Exp Med, 2021).

overall_design:
Autoimmune primary biliary cholangitis (PBC) was induced in C57Bl/6 mice as described before: Chang et al., 2014; Wakabayashi et al., 2008. Briefly, mice were immunized with 100 µg of 2-octynoic acid BSA conjugate (2OA-BSA) intraperitoneally (i.p.) in a mix of PBS and complete Freund’s adjuvant (CFA, Sigma-Aldrich) at day 0 and were reboosted at days 14 and 28 with 2OA-BSA and incomplete Freund’s Adjuvant (IFA, Sigma Aldrich). Concomitantly with the two first injections of 2OA-BSA, mice were also injected intravenously (i.v.) with 2 μg of α-galactosylceramide (α-GalCer, Abcam) in PBS.
Non-autoimmune primary sclerosing cholangitis model (PSC) was induced in C57Bl/6 mice as previously published: Fickert et al., 2007; Ikenaga et al., 2017. They were fed the SAFE A04 diet (SAFE™) containing 0.089% (in weight) of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC, Sigma-Aldrich) for 2 weeks (from day 0 to 14). After one week of recovery with the regular diet, mice were fed again with the DDC-supplemented diet for one more week.  For bulk mRNA-sequecing, 4 healthy/normal mouse livers, 3 PBC mouse livers, and 3 PSC mouse livers were collected at day 35 post-cholangitis induction (Paillet et al, J Exp Med, 2021).

first: Juliette

last: Paillet

first: Jonathan

last: Pol


title: Human  retinal   organoids release  extracellular vesicles  that  regulate  gene  expression in  target  human  retinal  progenitors

status: Public on Aug 27 2021

city: Bronx

first: Stephen

last: Redenti

state: NY

address: Biology Dept. , 250 Bedford Park Blvd.

institute: Lehman College, CUNY

summary: Developing human retinal organoids and their EVs contain unique populations of small noncoding RNAs, including miRNA, piRNA and tRNA. The EV genetic cargo has functions  correlated  to  retinal  differentiation  and  development.  Retinal   organoid   EVs   educate multipotent retinal progenitor cell differentiation toward photoreceptor and ganglion cell fates.

sample_organism:
Homo sapiens
blank sample

platform_organism:
Homo sapiens
blank sample

overall_design: Human retinal organoid EV miRNA cargo and their effect on target human retinal progenitor cells mRNA expression characterized.

first: Maria

middle: V

last: Canto-Soler


title: Human prostate cancer cell line, 22Rv1: Control vs. luteolin treatment

first: Aya

last: Naiki-Ito

address: 1-Kawasumi, Mizuho-cho, Mizuho-ku

department: Department of Experimental Pathology and Tumor Biology

institute: Nagoya City University Graduate School of Medical Sciences

summary: The miRNA expression profiling between Control and Luteolin in 22Rv1

overall_design: 22Rv1 cells were treated  25 μM luteolin for 48 hours.


title: Mechanistic dissection of dominant AIRE mutations in mouse models reveals evidence for AIRE auto-regulation

city: Rehovot

first: Jakub

last: Abramson

address: 234 Herzl st.

department: Department of Immunology

institute: Weizmann Institute of Science


title: The transcription factor NF-Y participates in stem cell fate decision and regeneration in adult skeletal muscle

city: Modena

first: Carol

last: Imbriano

address: Via Campi 213/D

department: Life Sciences

institute: University of Modena and Reggio Emilia

summary: The transcription factor NF-Y promotes cell proliferation and often loses its activity during differentiation through the regulation of NF-YA, the DNA binding subunit of the complex. In stem cell compartments, the shorter NF-YA splice variant (NF-YAs) is abundantly expressed and sustains their expansion. Here, we report that satellite cells, the stem cell population of adult skeletal muscle necessary for its growth and regeneration, express uniquely the longer NF-YA isoform (NF-YAl), majorly associated with cell differentiation. Through the generation of a conditional knock out mouse model that selectively ablates NF-YA in satellite cells, we demonstrate that NF-YA expression, and hence NF-Y activity, is fundamental to preserve the pool of muscle stem cells. Moreover, NF-Y supports their commitment to differentiation and ensures robust regenerative response to muscle injury. Gene expression profiling highlights an unexpected role for NF-Y in stem cell biology and opens a new scenario for NF-Y activity that is dispensable for muscle stem cell proliferation but required for efficient myogenic differentiation.

overall_design: Expression profile of Muscle Satellite Cells in NF-YA cell-specific conditional Knock Out Mice.

first: Giovanna

last: Rigillo


title: IGSF11 is required for pericentric heterochromatin dissociation during meiotic diplotene

city: Beijing

first: Jing

last: He

state: Beijing

address: Room D110, Medical Science Building, School of Medicine, Tsinghua University

department: School of Medicine

institute: Tsinghua University

summary: We compared the differences in transcriptional and chromatin structure between Igsf11 knockout or control mouse spermatocytes

overall_design: RNA-seq analysis of leptotene and pachytene spermatocytes from Igsf11 knockout or control mouse spermatocytes. Hi-C analysis of diplotene or abnormal spermatocytes from control or Igsf11 knockout mouse spermatocytes.

first: Bo

last: Chen

first: An

last: Yan

first: Yang

last: Liu


title: Epigenetic and transcriptomic profiling of neural stem cells after midazolam exposure

city: Ikoma

first: Taito

last: Matsuda

institute: Nara Institute of Science and Technology

summary: Here we show that early-life exposure to midazolam (MDZ), a widely used drug in pediatric anesthesia, persistently alters chromatin accessibility and expression of quiescence-associated genes in neural stem cells (NSCs) in mouse hippocampus. The alterations led to a continuous restriction of NSC proliferation toward adulthood, resulting in reduction of neurogenesis associated with the impairment of hippocampal-dependent memory functions. Moreover, we found that voluntary exercise restored hippocampal neurogenesis accompanied by the normalization of MDZ-perturbed transcriptome and ameliorated declined cognitive ability in MDZ-exposed mice.

overall_design: Nestin-EGFP mice were injected with 10mg/kg of MDZ or dH2O. RNA-seq and ATAC-seq was performed using EGFP-positive NSCs and their progenies isolated from Nestin-EGFP mice at 10-day-old (P10) and 8-week-old (8W) mice with or without voluntary exercise (RUN).  For ChIP-seq analysis, Egr1 was transduced in cultured NSC and collected samples were then subjected to ChIP assay using anti-FLAG antibody..

first: T

first: H

last: Doi

first: K

last: Nakashima


title: In-situ cell-type specific chromatin topologies in the brain revealed by genome architecture mapping [ATAC-seq]

city: Berlin

first: Alexander

last: Kukalev

address: Hannoversche Str., 28

department: Berlin Institute for Medical Systems Biology

institute: Max-Delbrueck Center for Molecular Medicine

summary: We report the application of genome architecture mapping in specific cell types in mouse brain. We generated cell-type specific chromatin contact maps in mouse dopaminergic neurons from the midbrain ventral tegmental area (VTA DN), pyramidal glutamatergic neurons from the cornus ammonis 1 region of the hippocampus (CA1 PGN), and non-neuronal post-mitotic oligodendrocytes from the somatosensory cortex (SSC_Olig). We explored cell-type specific chromatin topologies genome-wide at multiple genomic scales. Our data demonstrates that chromatin organization is cell type specific and reflects cell specialization at all genomic scales.

overall_design:
bulk mESC ATAC-seq; VTA snATAC-seq
Please note that the 'ATACseq_VTA*_DN' processed data was generated from both replicates and is linked to the ATACseq_VTA1_DN sample records.

first: Luna

middle: Z

last: Redondo

first: Izabela

last: Harabula

first: Warren

last: Winick-Ng

first: Ana

last: Pombo


title: RNAseq of mRNA from  murine small intestinal crypts

city: Munich

first: Monica

last: Yabal

address: Ismaninger straße 22

institute: Technical University of Munich

summary: Spontaneous inflammation in the terminal ileum of Xiap–/– mice was observed to occur in a microbiome dependent manner. Xiap–/– mice housed alone presented with signs of inflammation which were alleviated upon co-housing the mice with wild-type counterparts. To elucidate the impact of co-housing, and thus the transfer of the microbiome to affected Xiap–/– mice, crypts from the small intestine of these mice were analyzed.

overall_design: Small intestinal crypts from wild-type and Xiap-deficient mice either housed according to genotype or co-housed together for four weeks were isolated and subjected to RNA-seq analysis.

first: Sainitin

last: Donakonda

first: Rupert

last: Oellinger

first: Thomas

last: Engleitner


title: The role of interferon regulatory factor 8 for retinal tissue homeostasis and development of choroidal neovascularisation

city: Freiburg

first: Clemens

last: Lange

address: Kilianstraße 5

department: Klinik für Augenheilkunde

institute: Uniklinik Freiburg

summary: Microglia represent the resident innate immune cells of the retina and are important for retinal development and tissue homeostasis. However, dysfunctional microglia can have a negative impact on the structural and functional integrity of the retina under native and pathological conditions. In this study, we used interferon-regulating factor 8 (Irf8)-deficient mice to determine the transcriptional profile, morphology, and temporal-spatial distribution of microglia lacking Irf8 and to examine the effects on retinal development, tissue homeostasis, and choroidal neovascularization (CNV) formation. We hereby found a severely altered morphological phenotype accompanied by loss of microglia signature genes in IRF8 deficient microglia. An in-depth characterization by funduscopy, fluorescein angiography, optical coherence tomography and electroretinography revealed no major retinal abnormalities. However, in the laser-induced CNV model, Irf8-deficient microglia showed increased activity of biological processes critical for inflammation and cell adhesion and reduced cell number near the lesions, which was associated with significantly increased CNV lesion size. Our results suggest that Irf8 has negligible functions in the steady state but is critical in converting resident microglia to a reactive phenotype under pathologic conditions and thus can suppress retinal inflammation and CNV formation.

overall_design: RNA sequencing of retinal microglia from Irf KO mice without laser and Irf KO mice with laser

first: Peipei

last: Zhang

first: Anja

last: Schlecht

first: Julian

last: Wolf

first: Stefaniya

last: Boneva

first: Yannik

last: Laich

first: Jana

last: Koch

first: Franziska

last: Ludwig

first: Myriam

last: Böck

first: Adrian

last: Thien

first: Hansjürgen

last: Agostini

first: Günther

last: Schlunck

first: Marco

last: Prinz

first: Ingo

last: Hilgendorf

first: Peter

last: Wieghofer


title: CPD-seq map of UV damage formation in isolated human genomic DNA

city: Pullman

first: John

middle: J.

last: Wyrick

address: Biotechnology Life Sciences 241

department: School of Molecular Biosciences

institute: Washington State University

summary: UV-induced CPDs were mapped in isolated human genomic DNA following 80J/m2 of UVC irradiation

overall_design: UV-induced cyclobutane pyrimidine dimers (CPDs) were mapped across the genome of isolated genomic DNA from human NHF1 cells that was irradiated in vitro with UV dose of 80 J/m2 of UVC light.

first: Peng

last: Mao


title: UVDE-seq map of 6-4PP formation in normal human skin fibroblasts

summary: UV-induced 6-4PPs were mapped in normal human skin fibroblasts following 500J/m2 of UVC irradiation

overall_design: UV-induced [6-4]photoproducts (6-4PPs) were mapped across the genome of normal human skin fibroblasts (NHF1) cells after they were irradiated with a UV dose of 500 J/m2 of UVC light.

first: Kaitlynne

last: Bohm


title: Long-term Glatiramer Acetate Treatment Induces Subtle Changes in Microglial Transcriptome

city: Rochester

first: O'Banion

last: Kerry

state: United States of America

address: 601 Elmwood Ave

institute: University of Rochester

summary: In this study, we investigated the therapeutic potential of a well-tolerated immunomodulatory relapsing-remitting multiple sclerosis drug, glatiramer acetate (GA), on the 3xTg mouse model of Alzheimer's Disease. Briefly, we treated aged female 3xTg mice (>15 mo) weekly with 0.1 mg of GA for 8 weeks. We were able to observe an improvement in cognition and amelioration of amyloid pathology, which we attempted to correlate with changes in microglial transcriptome. To this end, we sorted microglia (CD45int CD11b+) from the hippocampi of GA or PBS-treated 3xTg mice for bulk RNA-seq.

overall_design: Microglia (CD45int CD11b+) were sorted from isolated hippocampi and processed for bulk RNAseq.

first: Berke

last: Karaahmet

first: Dawling

last: Dionisio Santos

last: Olschowka

first: Kerry

last: O’Banion


title: PD-1+ Tcf1+ CD8+ T cells from established chronic infections can convert into memory cells but keep a stable imprint of persistent stimulation

city: Lausanne

first: Tania

last: Wyss

address: Rue du Bugnon 25A

institute: SIB Swiss Institute of Bioinformatics

summary: The CD8+ T cell response to chronic viral infection is sustained by virus-specific memory-like (TML) CD8+ T cells. TML have recall expansion, self-renewal and differentiation capacity, similar to central memory (TCM) CD8+ T cells that arise in response to acute infection and persist long-term in the absence of antigen. An unresolved question is whether TML can also form memory. Here we showed that TML persisted in antigen free hosts. Further, in response to acute restimulation, TML expanded and differentiated inefficiently, but self-renewal and long-term persistence was not very different from TCM. Progeny of TML resembled conventional memory cells but retained multiple characteristics of chronically stimulated cells. This imprint was accounted for by the overexpression of the transcription factor Tox. Our findings demonstrated that chronically stimulated CD8+ T cells yielded memory that, however, differed from conventional memory formed in response to acute resolved infection.

overall_design: B6 mice (CD45.1/.2) and TCR Vb5 transgenic mice (CD45.1) were transferred with Tcf7GFP P14 cells from naive mice (CD45.2) and infected with LCMV Armstrong (Arm) and LCMV clone 13 (cl13), respectively. Total P14 cells were flow sorted at d32 post infection. Alternatively, Tcf7GFP+ P14 cells were flow sorted at d45 post Arm and cl13 infection and transferred into secondary B6 mice (CD45.1/.2) that were infected with LCMV Arm. Total P14 cells were flow sorted at d42 post infection (Tcm>Arm) and (Tml>Arm). Each sample derived from a pool of at least 3 mice.

first: Mélanie

last: Charmoy

first: Mauro

last: Delorenzi

first: Werner

last: Held